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Published on March 21, 2008; 10.1104/pp.108.117978

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Received February 18, 2008
Accepted March 16, 2008

Mild reductions in mitochondrial citrate synthase activity result in a compromised nitrate assimilation and reduced leaf pigmentation but have no effect on photosynthetic performance or growth

Agata Sienkiewicz-Porzucek , Adriano Nunes-Nesi , Ronan Sulpice , Jan Lisec , Danilo C. Centeno , Petronia Carillo , Andrea Leisse , Ewa Urbanczyk-Wochniak , and Alisdair R. Fernie *

Max-Planck-Institut fur Molekulare Pflanzenphysiologie, Am Muhlenberg 1, 14476 Golm, Germany; Dipartimento di Scienze della Vita, Seconda Universita degli Studi di Napoli, Via Vivaldi, 43 I-81100 Caserta, Italy

* Corresponding author; email: fernie{at}mpimp-golm.mpg.de.

Transgenic tomato (Solanum lycopersicum) plants, expressing a fragment of the mitochondrial citrate synthase gene in the antisense orientation and exhibiting mild reductions in the total cellular activity of this enzyme, displayed essentially no visible phenotypic alteration from the wild type. A more detailed physiological characterization, however, revealed that although these plants were characterized by relatively few changes in photosynthetic parameters they displayed a decreased relative flux through the TCA cycle and an increased rate of respiration. Furthermore, biochemical analyses revealed that the transformants exhibited considerably altered metabolism, being characterized by slight decreases in the levels of organic acids of the TCA cycle, photosynthetic pigments and in a single line in protein content but increases in the levels of nitrate, several amino acids and starch. We additionally, determined the maximal catalytic activities of a wide range of enzymes of primary metabolism, performed targeted quantitative PCR analysis on all three isoforms of citrate synthase and a broader transcript profiling using the TOM1 microarray. Results from these studies confirmed that if the lines were somewhat impaired in nitrate assimilation, they were not severely affected by this, suggesting the presence of strategies by which metabolism is reprogrammed to compensate for this deficiency. The results are discussed in the context of CN interaction and inter-organellar co-ordination of metabolism.






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